Role of the adaptive immune system in spiral ganglion neuron degeneration after deafening
Year: 2020
Type: dissertation
Abstract: Hearing loss is the most common sensory abnormality. Auditory receptor cell (hair cell) loss is the most common cause of sensorineural hearing loss. Cochlear implant a neural prosthesis, can replace the auditory function of the hair cells. However, optimum functioning of the cochlear implant depends on the functionality of the neurons that connect hair cells with the brain, known as spiral ganglion neurons (SGNs). In human, and in many animal models, SGNs die after deafening. There are various hypotheses for the pathogenesis of this neurodegeneration. Lack of neurotrophic factors from hair cells and lack of electrical stimulation are few of them. In recent years, this field has seen emergence of a new hypothesis: the neuroinflammation hypothesis. It has been observed that after deafening there is significant inflammation in spiral ganglion after deafening. In this thesis, I tried to figure out whether this inflammation is neurotoxic. As we found that it is neurotoxic, we then asked the question whether this neurotoxic neuroinflammation is an innate immune response or an adaptive immune response. We have found that MHCII mediated presentation of some antigen from the spiral ganglion is causal to the SGN degeneration after deafening. These data suggest that MHCII mediated adaptive immune response is central to the pathogenesis of SGN degeneration after deafening.
DOI: 10.17077/etd.005614
Language: English
Subfield: Sensory Systems
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
OpenAlex ID: W4242146485